ATM kinase activity modulates ITCH E3-ubiquitin ligase activity.
Roma, Italy. In Oncogene, 25 Mar 2013
Ataxia Telangiectasia Mutated (ATM) kinase, a central regulator of the DNA damage response, regulates the activity of several E3-ubiquitin ligases, and the ubiquitination-proteasome system is a consistent target of ATM.
ATM controls meiotic double-strand-break formation.
New York City, United States. In Nature, 2011
Here we report that the number of meiotic DSBs in mouse is controlled by ATM, a kinase activated by DNA damage to trigger checkpoint signalling and promote DSB repair.
Mdm2 links genotoxic stress and metabolism to p53.
Shanghai, China. In Protein Cell, 2010
Mdm2's oncogenic activity is mainly mediated by p53, which is activated by various stresses, especially genotoxic stress, via Atm (ataxia telangiectasia mutated) and Atr (Atm and Rad3-related).
p53 control of bone remodeling.
Shanghai, China. In J Cell Biochem, 2010
Moreover, Atm, c-Abl, and Mdm2, upstream regulators of p53 in DNA damage response, regulate osteoblast differentiation and bone remodeling as well.
ATM activation and DNA damage response.
Brisbane, Australia. In Cell Cycle, 2007
Well before the gene (ATM) mutated in the human genetic disorder ataxia-telangiectasia (A-T) was described it was evident from the clinical, molecular and cellular phenotype of A-T that this gene would play a central role in the DNA damage response.